TY - JOUR
T1 - Effects of Fibrinogen Concentrate on Thrombin Generation, Thromboelastometry Parameters, and Laboratory Coagulation Testing in a 24-Hour Porcine Trauma Model
AU - Zentai, Christian
AU - Solomon, Cristina
AU - van der Meijden, Paola E. J.
AU - Spronk, Henri M. H.
AU - Schnabel, Jonas
AU - Rossaint, Rolf
AU - Grottke, Oliver
PY - 2016/11
Y1 - 2016/11
N2 - Introduction: In a 24-hour porcine model of liver injury, we showed that fibrinogen supplementation does not downregulate endogenous fibrinogen synthesis. Here we report data from the same study showing the impact of fibrinogen on coagulation variables. Materials and Methods: Coagulopathy was induced in 20 German land race pigs by hemodilution and blunt liver injury. Animals randomly received fibrinogen concentrate (100 mg/kg) or saline. Coagulation parameters were assessed and thromboelastometry (ROTEM) was performed. Results: Fibrinogen concentrate significantly reduced the prolongations of EXTEM clotting time, EXTEM clot formation time, and prothrombin time induced by hemodilution and liver injury. A decrease in clot strength was also ameliorated. Endogenous thrombin potential was significantly higher in the fibrinogen group than in the control group, 20 minutes (353 24 vs 289 +/- 22 nmol/Lmin; P <.05) and 100 minutes (315 +/- 40 vs 263 +/- 38 nmol/Lmin; P <.05) after the start of infusion. However, no significant between-group differences were seen in other thrombin generation parameters or in d-dimer or thrombin-antithrombin levels. Fibrinogen-platelet binding was reduced following liver injury, with no significant differences between groups. No significant between-group differences were observed in any parameter at approximate to 12 and approximate to 24 hours. Conclusion: This study suggests that, in trauma, fibrinogen supplementation may shorten some measurements of the speed of coagulation initiation and produce a short-lived increase in endogenous thrombin potential, potentially through increased clotting substrate availability. Approximately 12 and 24 hours after starting fibrinogen concentrate/saline infusion, all parameters measured in this study were comparable in the 2 study groups.
AB - Introduction: In a 24-hour porcine model of liver injury, we showed that fibrinogen supplementation does not downregulate endogenous fibrinogen synthesis. Here we report data from the same study showing the impact of fibrinogen on coagulation variables. Materials and Methods: Coagulopathy was induced in 20 German land race pigs by hemodilution and blunt liver injury. Animals randomly received fibrinogen concentrate (100 mg/kg) or saline. Coagulation parameters were assessed and thromboelastometry (ROTEM) was performed. Results: Fibrinogen concentrate significantly reduced the prolongations of EXTEM clotting time, EXTEM clot formation time, and prothrombin time induced by hemodilution and liver injury. A decrease in clot strength was also ameliorated. Endogenous thrombin potential was significantly higher in the fibrinogen group than in the control group, 20 minutes (353 24 vs 289 +/- 22 nmol/Lmin; P <.05) and 100 minutes (315 +/- 40 vs 263 +/- 38 nmol/Lmin; P <.05) after the start of infusion. However, no significant between-group differences were seen in other thrombin generation parameters or in d-dimer or thrombin-antithrombin levels. Fibrinogen-platelet binding was reduced following liver injury, with no significant differences between groups. No significant between-group differences were observed in any parameter at approximate to 12 and approximate to 24 hours. Conclusion: This study suggests that, in trauma, fibrinogen supplementation may shorten some measurements of the speed of coagulation initiation and produce a short-lived increase in endogenous thrombin potential, potentially through increased clotting substrate availability. Approximately 12 and 24 hours after starting fibrinogen concentrate/saline infusion, all parameters measured in this study were comparable in the 2 study groups.
KW - blood coagulation factors
KW - bleeding
KW - hemostasis
U2 - 10.1177/1076029615584662
DO - 10.1177/1076029615584662
M3 - Article
C2 - 25948634
SN - 1076-0296
VL - 22
SP - 749
EP - 759
JO - Clinical and Applied Thrombosis-Hemostasis
JF - Clinical and Applied Thrombosis-Hemostasis
IS - 8
ER -